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Development, Plasticity, and Repair

Growth Cone Site of Axon Growth
Actin Cell Adhesion Molecules
Cadherins & N-Cams Actin that stick to other Cells
Integrins Stick to Laminin inside the cell
Actin Filaments Stabilize with Arp2/3
MAPs Stabilize microtubule Growth
PC12 w/ CSPG Barely grow
PC12 w/o CSPG Grow in many directions
First Stage of Neurite Outgrowth Spherical
Second Stage of Neurite Outgrowth Initial Sprouts
Third Stage of Neurite Outgrowth Immature Neurites
Growth Cone (Neurite outgrowth) Longest spine becomes the axon
Axons Don't taper
Dendrites Have many branches and taper
Growth Cone Cone Rich in Actin
Growth Cone Neurite Rich in Tubulin
Filopodia Extensions of actin
Integrin and Laminins What Filopodia look for
Matrix Adhesion Follows the Highest concentration of integrin and laminins
Cell Surface Adhesion Follows proteins expressed by other cells
Fasciculation Follows axon of another cell
GEF Guanazine Exchange Factor
Peripheral Growth Cone Domain Has Lamellipodia and Filopodia
Lamellipodia Sheet of Cell Membrane with F-Actin
Central Growth Cone Domain Nearest axon and contains cytoskeleton
Axon Shaft Permanent structure that will not change
Transitional Growth Cone Domain Thin region between peripheral and central
F-Actin Arc Generates force for the filopodia
Protrusion Actin bridges of filopodia extend
Engorgement Central Domain moves forward
Consolidation Axon shaft forms
Netrin in Growth Increases growth regardless of direction
Integrin in Growth Increases growth speed
Repulsion Cue F-Actin Retrograde Flow
Attractive Cue F-Actin assembly
ARP-23 Growth at angles along the length
Chemoattraction Follows a high concentration of chemicals
Contact Inhibition Follows the opposite direction of hitting something
Chemorepulsion Follows away from specific chemicals
Ephrin Pathway Activates RhoA, Rock, MLCK, and LIMK. Leads to Growth Cone Collapse
RhoA Makes GTP
Netrin Pathway Activates F-Actine Polymerization
Slit Pathway Activates Robo and builds growth cone
Semaphorin Pathway Deactivates RhoA
Semaphorin Sema1a interacts with tyrosine kinase
Netrin Directs growth of Neurons
Open Book Experiment By moving floor plates, proof neurons grow through plate, then away from
Netrin Receptors DCC and UNC-5
DCC Leads to attraction
UNC-5 Blocks DCC
Slit and Robo Interacts with DCC to change netrin from attractive to repulsive
Synaptogenesis When Axon comes into contact with Dendrite
Canonical Wnt Uses Gene transcription to form synapse
Divergent Wnt Anything not canonical
Proof 1 Divergent =/= Transcription Blocking RNA lets the assembly continue
Proof 2 Divergent =/= Transcription Time course isn't consistent
GSK3B Phosphorylates B-Catenin
Dishevelled (Dvl) Blocks GSK3B
B-Catenin Phosphorylated version targets for destruction
MAP1B Sticks to Microtubules and bends them
APC Pushes Growth Cone Forward
Frizzled Stops growth of Growth Cone
Wnt Main Effect Blocking GSK3B to prevent MAP1B phosphorylation
7a Wnt Recruits PSD-95
5a Wnt Alone, this makes inhibitory
5a and 7a Wnt Recruit JNK
PSD-95 Inserted by CaMKII and forms synapse
Microtubules Cytoskeleton Primary function is structural mainenance
Motor Proteins Walk down Microtubules
Microfilaments Made of actin that primarily are used to change the cell shape
Intermediate Filaments Used for cell shape tension
Dineds Two Feet Motor Proteins
Myosin One foot Motor Proteins
Benefit of Metabotropic Channel Crosstalk and Signal Increase
Acetylation Open up DNA
Methylation Closes up DNA
Regulator Elements Increase/Decrease Activation of DNA
Enhancer Sites Distal Control elements
Proximial Nearby Control Elements
Introns Junk DNA
Exons Actual DNA
RNA POLII Copies the DNA to RNA
Combinatory Control One gene is activated by a specific set of proteins
Poteolysis Destroys proteins with Ubiquitin
Activation Factors Have to come in contact by bending the DNA to the POLII
Drosophila Fruit Fly
C. Elegans Nemotode
C. Elegans Benefits Clear and Fate-Mapped
Forward Genetic Screen Looking for mutations
Reverse Genetic Screen Causing mutations
Knockout Prevent a Gene from Activating
Knockin Adding a Gene
Endoderm Becomes the Gut and Digestive Organs
Mesoderm Becomes the Muscles
Neuroectoderm Becomes Brain
Ectoderm Becomes Skin
Gastrulation Creates the Germ Layers
Neurulation Hollow Tube of Neural Tissue Formed
Delamination Cells individually migrate inside to become neural
Blastomere Cell derived from cleavage into early embryo
Blastula Structure made of blastomeres
Blastocoel Cavity where the Blastula is
Blastocyst Mammalian Blastula
Blastopore Invagination where Gastrulation begins
Nodochord Signaling Structure that tells prechordal plate to be neural
Floor Plate Signalling Structure
Neural Crest Formed at the edges of the plate
Archenteron Chamber where cells migrate inward
Epiblast Precursor to Early Embryo in Chick Egg
Area Pellucida Inner Flat Disk of Epiblast
Area Opaca Outer Flat Disk of Epiblast
Koller's Sickle Grows and forms Henson's Node
Henson's Node Migrates and leaves a trail of mesoderm
Primative Streak Becomes the mesoderm in Epiblast
What direction does Henson's Node move? Dorsal
Spina Bifida Neural Tube failure that leads to impairment
Cranioarchischisis No head
Anencephaly Brain doesn't fully form
Neural Induction One tissue causes a change in development of another
Specificiation Cell has information directing it to fate
Commitment Cell has committed to be a specific fate
BMP Signal for cells to become skin
CCNF Cerberus Chordin Noggin Follistatin Blocks BMP
SMAD Makes cells ectodermal. Blocked by CCNF
MAP Kinase Inactivates SMAD
Body Axis Formed by the Mesoderm
Bicroid Original Signal Gradient Cannot transcribe itself
Hunchback Reflects Initial Concentration of Bicoid
Dorsal Chemical that diffuses in the dorsal direction
Snail Chemical that turns cells to Mesoderm from High Dorsal
SOG Chemical that turns cells to neuroectoderm from Medium Dorsal
DPP Chemical that turns cells to Ectodermal
Gap Genes Order Kni, Till, gt, Kr, Kni, gt
Transcription Factor Combination Eve/Ftz+ Hunchback + Gap Genes = Body Regions
Hox Genes Homeobox Genes that are activated by Pair Rule and Gap Genes
AP Axis Defined by the direction of Hensen's Node
Competence Cells have the potential to reach this fate
Notch Makes other cells next to the neural cell skin
HES Makes Glia Cells
Motogenic Factors Initiation of Cell Migration MIA and Slits
Chain Migration Scaffold are made of cells that are migrating
Rostral Migratory Stream New olfactory neurons divide in subventricular zone
Symmetric Proliferative All Progenitors
Asymmetric Generative Rise of Neurons
Symmetric Generative Neurons overtake progenitors
Neural Crest Cells Originate at Neural Plate Border Become numerous tissue
Axon Initial Segment Where Action Potentials start
S4 Helix What moves and opens the voltage channels
Relative Refractory Period Harder to fire again
Ohm's Law Voltage = Current * Resistance
Synaptotagmin Twists SNARE
Quanta One vesicle release
Microdomains Concentrations of calcium near active zones
Binomial Distribution bin (x, n, p)
Bin X Number released
Bin N Number available to release
Bin P Probability of release
p * q Probability of one releasing, but not another
p^z * q^y Probability of a specific configuration
nCx n!/(n-x)!*x!
Habituation Decrease in amount of released Glutamate
Fewer docked vesicles Why habituation releases less glutamate
Low Calcium leves What causes habituation
Wnt Pathway: Wnt leads to Frizzled
Wnt Pathway: Frizzled leads to Dvl
Wnt Pathway: Dvl leads to GSK3B
Wnt Pathway: GSK3B leads to BK and MAP1B
Wnt Pathway: MAP1B leads to Looping Microtubules
HFS Rapid firing of the presynaptic neuron
Gs Enzyme PKA
Gq Enzyme PKC
Gi Enzyme None. Inhibits adenylyl cyclase
PKA affects Potassium Channels and Release Machinery
PKC Opens Calcium Channels
Sensitization uses the Gq Pathway
PLC Goes to PIP2 and removes IP3
IP3 Removal leaves behind DAG
DAG Activates PKC
Classical Conditioning Sensitization, but with association
Calmodulin acivates CaMKII and CaMKIV
Coincidence Detector in CC Adenylyl Cyclase
CREB Mediates Gene Transcription
MAPK and PKA Activates CREB
Mossy Fiber LTP No coincidence detector, but based on activity levels
Direct Pathway Starts in Layer 3 of entorhinal
Trysynaptic Pathway Starts in Layer 2 of entorhinal
Mossy Fiber Pathway Leads to Schaffer Collateral
Schaffer Collateral Pathway Associative and calcium dependent
Mossy Fiber relies on which Enzyme? PKA (MF)
Commissural Pathway Requires Post Synaptic Involvement
PKC and AMPA 1 leads to insertion of 2
CaMKII Rapid Phosphorylation of existing receptors
L-Type Ca Channels Present in the Direct Perferant Pathway
Sensitization Pathway(s) Gs and Gq
Hebbian Synapse Cell A before Cell B leads to LTP. After leads to LTD
Anti-Hebbian Synapse Anything that's not Hebbian
Negative ^T Cell B is stimulated first
Positive ^T Cell A is stimulated first
PKA is needed for which LT_? LTP
GluN2B Required for fear conditioning
Basolateral Amygdala Site of signal convergence
Wallerian Degeneration Breaking down with no containing
Wild Degeneration Breaking down with containing
GP130 Required for Regeneration
SOCS3 Blocks Regeneration
Oligodentrocytes summons? Reactive Astroctyes and Macrophages/Microglial Cells
Schwann Cells Myelin in Peripheral
Neuroprogenetors Parent neuron for new neurons
Parkinson's Disease Loss of dopaminergic neurons
Substantia Nigra What is affected in Parkinson's
Calcinurin LTD Protein
Created by: Grezar15
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